The present invention generally relates to a programmable cardiac stimulation device for automatically monitoring capture, following the delivery of a stimulation pulse. More specifically, the stimulation device has the ability to distinguish fusion from a loss of capture during dual-chamber or multi-chamber stimulation.
In healthy human heart, the sinus node, generally located near the junction of the superior vena cava and the right atrium, constitutes the primary natural pacemaker initiating rhythmic electrical excitation of the heart chambers. The cardiac impulse arising from the sinus node is transmitted to the two atrial chambers, causing a depolarization known as a P-wave and the resulting atrial chamber contractions. The excitation pulse is further transmitted to and through the ventricles via the atrioventricular (A-V) node and a ventricular conduction system, causing a depolarization known as an R-wave and the resulting ventricular chamber contractions. Disruption of this natural pacemaking and conduction system as a result of aging or disease can be successfully treated by artificial cardiac pacing using implantable cardiac pacing devices, including pacemakers and implantable defibrillators, which deliver rhythmic electrical pulses or anti-arrhythmia therapies to the heart at a desired energy and rate. One or more heart chambers may be electrically paced depending on the location and severity of the conduction disorder.
Modern pacemakers and implantable defibrillators possess numerous operating parameters, such as pacing pulse energy, base pacing rate, sensing threshold, pacing mode, etc., that must be programmed by the physician to satisfy individual patient need. In practice, this programming process can be time consuming and complicated. One goal of pacemaker manufacturers, therefore, has been to fully automate pacemaker function in order to minimize the complexity of programming operations and to maximize the safety and effectiveness of the cardiac pacing device.
One basic function of the pacemaker is to deliver a pacing pulse of sufficient energy to depolarize the cardiac tissue causing a contraction, a condition commonly known as xe2x80x9ccapture.xe2x80x9d Automating this function continues to be a strong focus of development efforts by pacemaker manufacturers. A straightforward approach to ensure capture is to deliver a fixed high-energy pacing pulse. While this approach, used in early pacemakers is simple, it quickly depletes battery energy and can result in patient discomfort due to extraneous stimulation of surrounding skeletal muscle tissue.
Therefore, a goal which is strived for in the pacemaker industry is to deliver pacing pulses at, or slightly higher than the pacing xe2x80x9cthreshold.xe2x80x9d Pacing threshold is defined as the lowest pacing pulse energy at which capture occurs. By stimulating the heart chambers at or just above threshold, comfortable and effective cardiac pacing is provided without unnecessarily depleting battery energy. Pacing threshold, however, is extremely variable from patient-to-patient due to variations in electrode systems used, electrode positioning, physiological and anatomical variations of the heart itself and so on.
Therefore, at the time of device implant, the pacing threshold is determined by the physician who observes an ECG recording while pulse energy is decreased, either by decrementing the pulse amplitude or the pulse width, until capture disappears. The pacing pulse energy is then programmed to a setting equal to the lowest pulse energy at which capture still occurred (threshold) plus some safety margin to allow for small fluctuations in the threshold. Selection of this safety margin, however, can be arbitrary. Too low of a safety margin may result in loss of capture, a potentially fatal result for the patient. Too high of a safety margin will lead to premature battery depletion and potential patient discomfort.
Furthermore, pacing threshold will vary over time within a patient due to fibrotic encapsulation of the electrode that occurs during the first few weeks after surgery; fluctuations that may occur over the course of a day, with changes in medical therapy or disease state and so on. Hence, techniques for monitoring the cardiac activity following delivery of a pacing pulse have been incorporated in modern pacemakers in order to verify that capture has indeed occurred. If a loss of capture is detected by such xe2x80x9ccapture-verificationxe2x80x9d algorithms, a threshold test is performed by the cardiac pacing device in order to re-determine the pacing threshold and automatically adjust the pacing pulse energy. This approach, as embodied in the Pacesetter, Inc. AUTOCAPTURE(trademark) Pacing System, improves the patient""s comfort, reduces the necessity of unscheduled visits to the medical practitioner, and greatly increases the pacemaker""s battery life by conserving the energy used to generate stimulation pulses.
A widely implemented technique for determining whether capture has occurred is monitoring the myocardial or intra-cardiac electrogram (EGM) received on the cardiac pacing and sensing electrodes. Heart activity is monitored by the pacemaker by keeping track of the stimulation pulses delivered to the heart and examining the EGM signals that are manifest concurrent with depolarization or contraction of muscle tissue (myocardial tissue) of the heart. The contraction of atrial muscle tissue is evidenced by generation of a P-wave, while the contraction of ventricular muscle tissue is evidenced by generation of an R-wave (sometimes referred to as the xe2x80x9cQRSxe2x80x9d complex). Through sampling and signal processing algorithms, the presence of an xe2x80x9cevoked responsexe2x80x9d following a pacing pulse is determined. The xe2x80x9cevoked responsexe2x80x9d is the depolarization of the heart tissue in response to a stimulation pulse, in contrast to the xe2x80x9cintrinsic responsexe2x80x9d which is the depolarization of the heart tissue in response to the heart""s natural pacemaking function.
When capture occurs, the evoked response is an intracardiac P-wave or R-wave that indicates contraction of the respective cardiac tissue in response to the applied stimulation pulse. For example, using such an evoked response technique, if a stimulation pulse is applied to the ventricle (hereinafter referred to as a Vpulse), a response sensed by ventricular sensing circuits of the pacemaker immediately following application of the Vpulse is presumed to be an evoked response that evidences capture of the ventricles.
However, it is for several reasons very difficult to detect a true evoked response. One problem commonly encountered during capture verification is xe2x80x9cfusion.xe2x80x9d Fusion occurs when a pacing pulse is delivered such that the evoked response occurs coincidentally with an intrinsic depolarization. The evoked signal may be absent or altered preventing correct capture detection by the pacemaker""s capture detection algorithm. A loss of capture may be indicated when capture is in fact present, which is an undesirable situation that will cause the pacemaker to unnecessarily deliver a high-energy back-up pacing pulse and to invoke the threshold testing function in a chamber of the heart. Frequent delivery of back-up pacing pulses or execution of threshold tests defeats the purpose of the energy-saving features of AUTOCAPTURE(trademark). If fusion continues during a threshold test, the pacing energy output may be driven to a maximum level, quickly depleting the battery energy.
The incidence of fusion can be particularly problematic in patients with intermittent or intact atrio-ventricular conduction being treated by dual-chamber pacing. In dual-chamber pacing, both atrial and ventricular activity are monitored. A P-wave detected in the atria is followed by an AV/PV interval, which is the desired delay between an atrial depolarization and a ventricular depolarization. If an intrinsic R-wave is not detected prior to expiration of the AV/PV delay, a Vpulse is delivered to pace the ventricles. Since the AV conduction time may vary, an intrinsically conducted R-wave may occur at different times and therefore may occur approximately the same time that a ventricular pacing pulse is delivered. Furthermore, the AV/PV interval may be programmed inappropriately leading to increased likelihood of fusion events. Fusion masquerading, as loss of capture will cause the pacemaker to initiate frequent threshold tests and may drive the pacemaker to its maximum pacing output.
Rate variability, particularly in rate-responsive pacemakers, may further complicate timing sequences. In rate-responsive pacemakers, the pacing interval automatically shortens in response to increased metabolic demand. However, the AV interval may not be shortened accordingly resulting in increased likelihood of fusion.
To address the problem of fusion, techniques have been proposed to shorten the pacing interval subsequent to a loss of capture. By pacing earlier, fusion is less likely to occur during future pacing cycles. Reference is made for example to U.S. Pat. Nos. 4,969,462 and 4,969,467 to Callaghan et al.
In order to verify that fusion has occurred, a method has been proposed to make use of the physiological refractory time of cardiac tissue. Reference is made for example to U.S. Pat. No. 4,955,376 to Callaghan et al. This method takes advantage of the fact that once cardiac tissue has been depolarized, it cannot be depolarized again until the ion flow that has occurred across the cardiac cell membrane during the first depolarization has returned to the resting state. This time period is known as refractory. If a high-energy back-up pacing pulse is delivered during the physiologic refractory period, no depolarization will result. Therefore, if a high-energy pacing pulse delivered soon after a loss of capture does not elicit an evoked response, the loss of capture was likely to have been a fusion event that was misdetected. On the other hand, if an evoked response is detected following the back-up pacing pulse, then the loss of capture detection is accurate. The back-up pacing pulse is necessary for the implementation of this method, and is followed by an automatic threshold test. However, the delivery of a high-energy pacing pulse for verifying the occurrence of fusion uses precious battery life without direct therapeutic benefit.
Zhu et al. provide a method in U.S. Pat. No. 6,038,474 for avoiding fusion during auto-capture regimes by delivering a xe2x80x9cpre-lookxe2x80x9d pacing pulse in order to determine if a fusion event is mistaken for a loss of capture. This approach requires the delivery of an additional pulse in order to avoid or verify fusion. Delivery of this additional pacing pulse does not fully conform to the overall energy-savings intent of AUTOCAPTURE(trademark) regimes.
The difficulty heretofore, is the inability to reliably detect when fusion occurs, without expending energy on back-up or pre-look pacing pulses and automatic threshold tests. The difficulty in detecting fusion arises from polarization effects on the electrodes used for both pacing and sensing, and the alteration of the evoked response during fusion, making it undetectable by the normal capture verification regimes. Hence, fusion is misinterpreted as a loss of capture by the ventricular channel.
However, a signal associated with the ventricular R-wave is also detectable on the atrial channel, known as a xe2x80x9cfar-fieldxe2x80x9d R-wave, or FFR. FFR signals are generally ignored, and oftentimes avoided, on the atrial channel by applying blanking and refractory intervals following the delivery of a Vpulse because far-field signals might otherwise be inaccurately interpreted as atrial events. However, detection of a FFR on the atrial channel during fusion would provide a way of determining that fusion has occurred without delivering additional pacing pulses. The FFR signal resulting from a normal R-wave and during a fusion event is similar in morphology. Therefore, detection of a FFR on the atrial channel when loss of capture occurs on the ventricular channel would be a useful means for detecting fusion.
It would thus be desirable, particularly in dual-chamber pacemakers, to provide a system and method for accurately detecting fusion events. Furthermore, it would be desirable to detect fusion without requiring delivery of additional pacing pulses, particularly high-energy pacing pulses.
The present invention addresses these and other problems by providing a multi-chamber stimulation device that reliably and automatically distinguishes fusion from loss of capture during ventricular stimulation.
One feature of the present invention is to provide immediate and accurate fusion detection when a loss of capture is suspected in the ventricles without delivering back-up stimulation pulses. To achieve this objective, the far-field signal present in the atrial channel is examined for evidence of a FFR (far-field R-wave) whenever the ventricular channel detects a loss of capture. If a FFR is present, fusion is confirmed. If a FFR is absent, loss of capture is confirmed.
An additional feature of the present invention is the inhibition of a back-up stimulation pulse upon fusion detection. A high-energy back-up stimulation pulse is normally generated by the ventricular channel when loss of capture is detected. By correctly distinguishing fusion from a loss of capture, back-up stimulation can be inhibited as well as the normally invoked threshold test. Hence, the present invention provides an important energy-savings feature.
Yet another feature of the present invention is the automatic adjustment of stimulation parameters whenever fusion is confirmed, so that fusion can be avoided on future paced beats or during future threshold tests. Thus, the present invention improves the performance of the pacemaker device by properly distinguishing fusion from loss of capture and responding appropriately to both situations.
Therefore, the present invention achieves several objectives, among which are the following: 1) accurate detection of fusion immediately upon its occurrence, without delivering additional stimulation pulses; 2) inhibition of unnecessary back-up stimulation and threshold tests when fusion occurs; and 3) appropriate adjustment of stimulation parameters based on confirmed fusion detection such that fusion recurrence is minimized.